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Introduction

Fecal incontinence is a diagnosis represented by recurrent uncontrolled passage of fecal material for at least 3 months. It is relatively common, with an assumed prevalence of up to 7% of the worldwide population. The therapy is challenging and often with insufficient clinical results. It should be specifically tailored to different symptom presentations meaning urge or passive incontinence. One of the relatively and therefore not widely used treatment options for incontinence is local sphincter stimulation which is a safe non or minimally invasive method. This stimulation could be performed in at home setting, so it presents a substantial time and cost-saving option for the patient and for the healthcare system. However, the data published on this topic so far are scarce with heterogeneous studied populations and results with no universally accepted treatment protocol.

Aims & Methods

This study aims to evaluate the effect of local sphincter stimulation on the functional parameters of sphincters and symptoms based on the different phenotypes. This is a retrospective single-center study analysis on patients with fecal incontinence (age> 18 years). The duration of the training was 12 weeks, with training once daily for 6 days a week. The parameters of the home stimulation device were as follows: Frequency: 40 Hz; Impulse Width: 0.2 s; Ramp-up time: 1s; Workout time: 6s; Rest: 15s. Training duration: 20min. During the perceived stimulation patients were instructed to squeeze the sphincter. 3D anorectal manometry was performed according to the IAPWG protocol at the initiation visit and the control visit. Clinical evaluation was performed by self-reporting Wexner’s score for fecal incontinence at both visits.

Results

Twenty-three patients (23) were consecutively screened for eligibility and assigned for the therapy. Three patients (3) did not adhere to the training due to various personal reasons one (1) patient did not tolerate stimulation. Therefore, 19 patients (10 passive, 9 urge) completed the full treatment protocol for 12 weeks and were considered for the final analysis. The total average increase in sphincter rest medium pressure was 22.53%, with significantly higher improvement in the urge group compared to the passive group (46.24% vs. 1.18% respectively). The total average increase in sphincter rest maximum pressure was 25.69%, with significantly higher improvement in the urge group compared to the passive group (46.92% vs. 6.59% respectively). The total average increase in sphincter maximum squeeze pressure was 36.13%, with significantly higher improvement in the urge group compared to the passive group (57.82% vs. 16.61% respectively). The average improvement in Wexner score was 3.1 points, with higher improvement in the urge group compared to the passive group (4.2 points vs. 2.1 points respectively).

Conclusion

The home-administered local anal sphincter stimulation for 12 weeks seems to be an effective treatment option for both types of fecal incontinence and significantly more effective in the urge type. Therefore this could be considered as a cost and time-effective treatment option compared to standard office-based therapy. Although a home stimulation device is simple to use, the ability of the patient to adhere to the protocol should be evaluated during the screening process.
Funding: European Parliament and Council Recovery and Resilience Plan of the Slovak Republic 2021 – 2027, code: 09I03-03-V04-00761

DIFFERENT EFFECT OF LOCAL SPHINCTER STIMULATION ON ANAL FUNCTION AND SYMPTOMS OF URGE VS. PASSIVE FECAL INCONTINENCE

Peter Liptak 1, Branislav Malý 1, Marek Vojtko 1, Peter Banovcin 1

1 Jessenius faculty of Medicine in Martin, Comenius University, Slovakia, Martin, Slovakia

Conference

UEG Week Berlin 2025

Topics

Colorectal

Submission format

Abstract

Session

LOWER GI (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Reflux: Paediatric and adult gastroenterologist

Alexandra Papadopoulou 1, Daniel Sifrim 2

1 University of Athens, Athens, Greece

2 Queen Mary University London, Blizard Institute, London, United Kingdom

Event

UEG Week Berlin 2025

Session

When adult gastroenterologist meets paediatrician: Focus on reflux, constipation and chronic pain

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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EMR or ESD for duodenal adenoma: Too much recurrence and too much risk?

Marc Barthet 1, Naohisa Yahagi 2

1 Hopital Nord, Marseille, France

2 Keio University Cancer Center - Cancer Center, Keio University Cancer Center; Tokyo/JP, Tokyo, Japan

Event

UEG Week Berlin 2025

Session

Never waste a good disaster

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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MICROPLASTIC-INDUCED ALTERATIONS IN GUT MICROBIOME AND METABOLISM: INSIGHTS FROM AN EX VIVO BIOREACTOR MODEL

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Introduction

Microplastic particles (MPs), defined as plastic fragments smaller than 5 mm, are pervasive pollutants that accumulate in ecosystems and the human food chain (1). Literature points at various health risks, including the induction of carcinogenesis (2). Emerging evidence from animal models (3) suggests that MPs may influence the gut microbiome, but the impact on the human gut microbiome remains poorly understood.

Aims & Methods

This study aimed to evaluate how various MP types influence gut microbial composition and metabolism using an ex vivo bioreactor model, with a focus on exploring potential carcinogenic effects arising from MP–microbiome interactions.
Stool samples from healthy donors were used to inoculate bioreactor cultures, which were maintained under anaerobic conditions for five days with daily nutrient feeding. These cultures were exposed to five common MP types—polystyrene (PS), polypropylene (PP), low-density polyethylene (LDPE), poly(methyl methacrylate) (PMMA), and polyethylene terephthalate (PET)—at concentrations mimicking both estimated human exposure (4) and higher doses to assess dose-dependence. Cell viability and total bacterial counts, as well as culture pH, were measured throughout the experiment. To further explore potential microbiome and metabolic alterations, 16S rRNA gene sequencing and targeted metabolomics were performed.

Results

MP exposure did not lead to significant changes in total or viable bacterial cell counts. However, MP-treated cultures exhibited a consistent and significant decrease in pH compared to controls, suggesting changes in microbial metabolic activity. Microbiome sequencing revealed plastic-type-dependent alterations in microbial composition, with certain bacterial taxa increasing or decreasing in abundance depending on the MP type. These shifts occurred across multiple genera within diverse families, including Lachnospiraceae, Oscillospiraceae, Enterobacteriaceae, and Ruminococcaceae, with the majority of changes occurring withing the phylum Bacillota. These compositional changes were accompanied by shifts in the metabolomic profiles, some of which correlated with the observed pH changes. Several plastic types induced changes in valeric acid levels, while individual MP types were associated with alterations in distinct metabolites such as uracil, lactic acid, and acetic acid.

Conclusion

This study demonstrates that MPs can affect gut microbial activity and metabolism without significantly altering overall bacterial abundance in the short term. The variation in microbiome response across plastic types highlights the complexity of MP-microbiome interactions. Changes in faecal pH are known to be associated with various gastrointestinal diseases (5). Interestingly, some of the MP-induced changes in microbial composition resembled patterns linked to diseases such as depression and colorectal cancer. In contrast, other changes showed patterns that differed from those typically associated with conditions like Parkinson’s disease and irritable bowel syndrome, highlighting the complexity of these associations and the dependency on the context. The bioreactor model provided a controlled environment for identifying direct MP-microbiome interactions; however, in humans, additional factors like diet, immune response, and individual microbiome variations play a role in determining long-term effects. Exposure duration may also play a critical role in shaping the extent and nature of microbiome alterations (6), underscoring the need for further research into the effects of chronic MP exposure and associated health risks.

References

(1) Mamun, A. A., Prasetya, T. A. E., Dewi, I. R., & Ahmad, M. (2023). Microplastics in human food chains: Food becoming a threat to health safety. The Science of the total environment, 858(Pt 1), 159834. https://doi.org/10.1016/j.scitotenv.2022.159834
(2) Kumar, R., Manna, C., Padha, S., Verma, A., Sharma, P., Dhar, A., Ghosh, A., & Bhattacharya, P. (2022). Micro(nano)plastics pollution and human health: How plastics can induce carcinogenesis to humans?. Chemosphere, 298, 134267. https://doi.org/10.1016/j.chemosphere.2022.134267
(3) Hirt, N., & Body-Malapel, M. (2020). Immunotoxicity and intestinal effects of nano- and microplastics: a review of the literature. Particle and fibre toxicology, 17(1), 57. https://doi.org/10.1186/s12989-020-00387-7
(4) Senathirajah, K., Attwood, S., Bhagwat, G., Carbery, M., Wilson, S., & Palanisami, T. (2021). Estimation of the mass of microplastics ingested - A pivotal first step towards human health risk assessment. Journal of hazardous materials, 404(Pt B), 124004. https://doi.org/10.1016/j.jhazmat.2020.124004
(5) Yamamura, R., Inoue, K. Y., Nishino, K., & Yamasaki, S. (2023). Intestinal and fecal pH in human health. Frontiers in Microbiomes, 2, 1192316.
(6) Yin, L., Yang, M., Teng, A., Ni, C., Wang, P., & Tang, S. (2025). Unraveling Microplastic Effects on Gut Microbiota across Various Animals Using Machine Learning. ACS nano, 19(1), 369–380. https://doi.org/10.1021/acsnano.4c07885

MICROPLASTIC-INDUCED ALTERATIONS IN GUT MICROBIOME AND METABOLISM: INSIGHTS FROM AN EX VIVO BIOREACTOR MODEL

Christian Pacher-Deutsch 1, Kristina Žukauskaitė 1, Cigdem Akar 2, Maximilian Nepel 2, Lukas Kogler 3, Hansjörg Habisch 2, Serena Ducoli 4, Stefania Federici 4, Tobias Madl 5, Verena Pichler 6, Angela Horvath 1, Vanessa Stadlbauer 7

1 Center for Biomarker Research in Medicine (CBmed), Graz, Austria|||Medical University of Graz, Graz, Austria

2 Medical University of Graz, Graz, Austria

3 Center for Biomarker Research in Medicine (CBmed), Graz, Austria|||University of Vienna, Vienna, Austria|||Medical University of Vienna, Vienna, Austria

4 University of Brescia, Brescia, Italy

5 Medical University of Graz, Graz, Austria|||BioTechMed-Graz, Graz, Austria

6 Center for Biomarker Research in Medicine (CBmed), Graz, Austria|||University of Vienna, Vienna, Austria

7 Center for Biomarker Research in Medicine (CBmed), Graz, Austria|||Medical University of Graz, Graz, Austria|||BioTechMed-Graz, Graz, Austria

Event

UEG Week Berlin 2025

Topics

Gut Microbiota Colorectal

Submission format

Abstract

Session

The gut ecosystem: From pathogenesis to treatment

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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RESTORING INTESTINAL BARRIER FUNCTION WITH GALLIC ACID: ORGANOID-BASED TRANSCRIPTOMIC AND PERMEABILITY ANALYSES

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Introduction

Epithelial barrier dysfunction is a hallmark of inflammatory bowel diseases (IBD), contributing to increased permeability, microbial translocation, and sustained mucosal inflammation^1,2. Targeting barrier restoration has emerged as a promising therapeutic strategy³. Gallic acid, a dietary polyphenol with known anti-inflammatory and antioxidative properties, has shown potential in modulating mucosal responses⁴. To investigate its impact on epithelial integrity under inflammatory stress, we utilized intestinal organoids as a physiologically relevant ex vivo model system.

Aims & Methods

The aim of this study was to investigate the potential of gallic acid to restore intestinal epithelial barrier function under inflammatory conditions, using colonic epithelial organoids and integrating transcriptomic and permeability analyses.
The study was approved by the Kaunas Regional Biomedical Research Ethics Committee (protocol no. BE-2-31). Inflamed differentiated colonic epithelial organoids were established from a patient with ulcerative colitis (UC) and non-IBD control individual by exogenous stimulation with TNF-α and IFN-γ (10 ng/mL each) for 24 hours. For gallic acid (GA) screening, organoids were pre-treated with metabolite (100 μM) for 1 hour prior to inflammation induction and co-treated during the induction period. Subsequently, organoids were either processed for mRNA sequencing (1×75 bp, NextSeq 550, Illumina) or subjected to a FITC-Dextran (4kDa) assay. RNA-seq data was processed, analyzed, and visualized using nf-core/RNAseq pipeline and RStudio. Images for permeability assay analysis were acquired using an inverted fluorescence microscope (Zeiss Axio Observer 7), processed with ImageJ, and analyzed and visualized in RStudio.

Results

Principal component analysis of transcriptomic profiles from both UC and non-IBD organoids revealed clear sample clustering driven by stimulation. Differential gene expression and Gene set enrichment (GSEA) analyses indicated a more pronounced cell response to both treatments in UC organoids compared to non-IBD organoids. Inflammation activated immune (CXCL9/10/11, CX3CL1), interferon (IFI44, SOCS1, NOS2), and defense genes (GBP4, GBP5, OAS2), while downregulating metabolic genes (FABP6, CFTR, HMGCS2) in both groups. Gene Ontology-based GSEA confirmed immune pathway enrichment and lipid metabolism suppression in inflamed cultures. In total, 3,148 and 1,479 DEGs were identified in inflamed UC and non-IBD organoids, respectively. GA treatment modulated 2,144 and 384 genes (e.g., LYPD8, MKI67, MT-ATP6, CXCL14, CCL22) in these groups, suggesting potential to rebalance inflammation and metabolism. GA co-treatment enhanced epithelial integrity in UC organoids via upregulation of cell junction, peptide hormone processing, and immune-related pathways. In non-IBD organoids, GA promoted cell adhesion pathways, supporting epithelial cohesion. Functional permeability analysis confirmed GA’s protective role, as supported by transcriptomic data. Mean percentages of FITC-Dextran-permeable organoids were 16.02% (untreated), 86.08% (inflamed), and 42.58% (inflamed + GA). A trend toward statistical significance (Wilcoxon p = 0.125) was observed in both untreated vs. inflamed and inflamed vs. inflamed + GA comparisons.

Conclusion

In conclusion, gallic acid modulates inflammatory and metabolic pathways during colonic inflammation and enhances epithelial barrier integrity.
Study was funded by the European Union and the State Secretariat for Education, Research and Innovation (SERI) (project: miGut-Health, grant no. 101095470).

References

¹Jostins, L., et al. (2012). Host–microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature, 491(7422), 119–124. https://doi.org/10.1038/nature11582
²Cleynen, I., et al. (2016). Inherited determinants of Crohn’s disease and ulcerative colitis phenotypes: A genetic association study. The Lancet, 387(10014), 156–167. https://doi.org/10.1016/S0140-6736(15)00465-1
³Vieujean, S., et al. (2025). Understanding the therapeutic toolkit for inflammatory bowel disease. Nature Reviews Gastroenterology & Hepatology. Online ahead of print. https://doi.org/10.1038/s41575-024-01035-7
⁴Tian, B., Ye, P., Zhou, X., Hu, J., Wang, P., Cai, M., Yang, K., Sun, P., & Zou, X. (2025). Gallic acid ameliorated chronic DSS-induced colitis through gut microbiota modulation, intestinal barrier improvement, and inflammation. Molecular Nutrition & Food Research. Online ahead of print. https://doi.org/10.1002/mnfr.70024